SAP controls T cell responses to virus and terminal differentiation of TH2 cells.

Journal article

SH2D1A, which encodes signaling lymphocyte activation molecule (SLAM)-associated protein (SAP), is altered in patients with X-linked lymphoproliferative disease (XLP), a primary immunodeficiency. SAP-deficient mice infected with lymphocytic choriomeningitis virus had greatly increased numbers of CD8+ and CD4+ interferon-gamma-producing spleen and liver cells compared to wild-type mice. The immune responses of SAP-deficient mice to infection with Leishmania major together with in vitro studies showed that activated SAP-deficient T cells had an impaired ability to differentiate into T helper 2 cells. The aberrant immune responses in SAP-deficient mice show that SAP controls several distinct key T cell signal transduction pathways, which explains in part the complexity of the XLP phenotypes.

Authors: Wu, C; Nguyen, K; Pien, G; Wang, N; Gullo, C

• Publication status: Published
• Journal: Nature immunology
• Volume: 2
• Issue: 5
• Pages: 410-414
• Publication date: 2001-05-01
• DOI: 10.1038/87713
• EISSN: 1529-2916
• ISSN: 1529-2908
• Language: English
• Keywords: Spleen; CD4-Positive T-Lymphocytes; Cytokines; Liver; CD8-Positive T-Lymphocytes; Cell Differentiation; T-Lymphocytes; Intracellular Signaling Peptides and Proteins; Signal Transduction; Immunoglobulin E; Carrier Proteins; Mice; Lymphocytic Choriomeningitis; Leishmaniasis, Cutaneous; Th2 Cells; Lymphoproliferative Disorders; Mice, Mutant Strains; Interferon-gamma; Animals